| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-127 |
Sentence |
denotes |
Molecular anatomy of an intracranial aneurysm: coordinated expression of genes involved in wound healing and tissue remodeling. |
| T2 |
128-151 |
Sentence |
denotes |
BACKGROUND AND PURPOSE: |
| T3 |
152-228 |
Sentence |
denotes |
Approximately 6% of human beings harbor an unruptured intracranial aneurysm. |
| T4 |
229-354 |
Sentence |
denotes |
Each year in the United States, >30 000 people suffer a ruptured intracranial aneurysm, resulting in subarachnoid hemorrhage. |
| T5 |
355-662 |
Sentence |
denotes |
Despite the high incidence and catastrophic consequences of a ruptured intracranial aneurysm and the fact that there is considerable evidence that predisposition to intracranial aneurysm has a strong genetic component, very little is understood with regard to the pathology and pathogenesis of this disease. |
| T6 |
663-671 |
Sentence |
denotes |
METHODS: |
| T7 |
672-974 |
Sentence |
denotes |
To begin characterizing the molecular pathology of intracranial aneurysm, we used a global gene expression analysis approach (SAGE-Lite) in combination with a novel data-mining approach to perform a high-resolution transcript analysis of a single intracranial aneurysm, obtained from a 3-year-old girl. |
| T8 |
975-1067 |
Sentence |
denotes |
RESULTS: SAGE-Lite provides a detailed molecular snapshot of a single intracranial aneurysm. |
| T9 |
1068-1287 |
Sentence |
denotes |
These data suggest that, at least in this specific case, aneurysmal dilation results in a highly dynamic cellular environment in which extensive wound healing and tissue/extracellular matrix remodeling are taking place. |
| T10 |
1288-1618 |
Sentence |
denotes |
Specifically, we observed significant overexpression of genes encoding extracellular matrix components (eg, COL3A1, COL1A1, COL1A2, COL6A1, COL6A2, elastin) and genes involved in extracellular matrix turnover (TIMP-3, OSF-2), cell adhesion and antiadhesion (SPARC, hevin), cytokinesis (PNUTL2), and cell migration (tetraspanin-5). |
| T11 |
1619-1631 |
Sentence |
denotes |
CONCLUSIONS: |
| T12 |
1632-1918 |
Sentence |
denotes |
Although these are preliminary data, representing analysis of only one individual, we present a unique first insight into the molecular basis of aneurysmal disease and define numerous candidate markers for future biochemical, physiological, and genetic studies of intracranial aneurysm. |
| T13 |
1919-2000 |
Sentence |
denotes |
Products of these genes will be the focus of future studies in wider sample sets. |
| T1 |
0-127 |
Sentence |
denotes |
Molecular anatomy of an intracranial aneurysm: coordinated expression of genes involved in wound healing and tissue remodeling. |
| T2 |
128-151 |
Sentence |
denotes |
BACKGROUND AND PURPOSE: |
| T3 |
152-228 |
Sentence |
denotes |
Approximately 6% of human beings harbor an unruptured intracranial aneurysm. |
| T4 |
229-354 |
Sentence |
denotes |
Each year in the United States, >30 000 people suffer a ruptured intracranial aneurysm, resulting in subarachnoid hemorrhage. |
| T5 |
355-662 |
Sentence |
denotes |
Despite the high incidence and catastrophic consequences of a ruptured intracranial aneurysm and the fact that there is considerable evidence that predisposition to intracranial aneurysm has a strong genetic component, very little is understood with regard to the pathology and pathogenesis of this disease. |
| T6 |
663-671 |
Sentence |
denotes |
METHODS: |
| T7 |
672-974 |
Sentence |
denotes |
To begin characterizing the molecular pathology of intracranial aneurysm, we used a global gene expression analysis approach (SAGE-Lite) in combination with a novel data-mining approach to perform a high-resolution transcript analysis of a single intracranial aneurysm, obtained from a 3-year-old girl. |
| T8 |
975-1067 |
Sentence |
denotes |
RESULTS: SAGE-Lite provides a detailed molecular snapshot of a single intracranial aneurysm. |
| T9 |
1068-1287 |
Sentence |
denotes |
These data suggest that, at least in this specific case, aneurysmal dilation results in a highly dynamic cellular environment in which extensive wound healing and tissue/extracellular matrix remodeling are taking place. |
| T10 |
1288-1618 |
Sentence |
denotes |
Specifically, we observed significant overexpression of genes encoding extracellular matrix components (eg, COL3A1, COL1A1, COL1A2, COL6A1, COL6A2, elastin) and genes involved in extracellular matrix turnover (TIMP-3, OSF-2), cell adhesion and antiadhesion (SPARC, hevin), cytokinesis (PNUTL2), and cell migration (tetraspanin-5). |
| T11 |
1619-1631 |
Sentence |
denotes |
CONCLUSIONS: |
| T12 |
1632-1918 |
Sentence |
denotes |
Although these are preliminary data, representing analysis of only one individual, we present a unique first insight into the molecular basis of aneurysmal disease and define numerous candidate markers for future biochemical, physiological, and genetic studies of intracranial aneurysm. |
| T13 |
1919-2000 |
Sentence |
denotes |
Products of these genes will be the focus of future studies in wider sample sets. |